1. Field of the Invention
The present invention relates to an implantable heart stimulator of the type having control means for controlling the delivery of stimulation pulses and an ischemia detector.
2. Description of the Prior Art
The aortic pressure is produced by the pumping action of the heart. During heart contraction--a systole--the blood pressure inside the heart is equal to or slightly higher than the pressure in the aorta, as long as the aortic valve is open and blood is flowing from the ventricle into the aorta or pulmonary artery. Between the contractions, that is during diastole, the aortic pressure is maintained by the elastic properties of the aortic wall. From the aorta, blood is circulated back to the heart via different parts of the body through the venous system. In this way blood is distributed to different organs of the body depending on the needs, the overall control of this distribution emanating from the autonomous nerve system.
Blood penetration of the heart is possible only in the diastolic phase when the aortic valve is closed. About 60% of the oxygen content inside the heart tissue is consumed during a heart contraction and in order to maintain the efficiency of the heart the consumed oxygen must be refilled till the next contraction.
The effect of an increased workload, due to e.g. movement of the patient, climbing stairs, running etc., is a higher blood flow in the body and a resulting increased need of energy and oxygen. This in its turn results in a more rapid decay of the aortic blood pressure between consecutive heart contractions. In response to such an increased demand a healthy heart is pumping at a higher rate and with an increased pumping force.
An increased heart rate results in only a minor shortening of the systolic phase, that is an increased heart rate results mainly in a shortening of the diastolic phase, which is the period during which oxygen is supplied to the heart as mentioned above.
An ischemic heart has a deficiency of oxygen because of insufficient blood to the heart tissue supply due to congestion and blocking of the coronary vessels by stenosis, emboli or spastic congestion. An increased workload will consequently worsen the situation for an ischemic patient.
In such a situation a symptomatic ischemia, that is angina pectoris, heart insufficiency or infarct, will force the patient, because of the associated pain, to stillness with a reduced heart rate as a consequence. This heart rate reduction can then at best stop the ischemic state.
No pacemaker system able to react on pain or any other ischemic indication is known. As a matter of fact pacemakers normally try to maintain a high stimulation rate, which is appropriate to a normal situation of the patient, and a so called rate response pacemaker system, responding to metabolical, haemodynamical or activity inputs will tend to increase the stimulation rate with increasing workload, thus worsening the ischemic situation of the patient.
In U.S. Pat. No. 5,199,428 a technique is described for detecting ischemia and both affecting stimulation of nerves regulating blood pressure and heart rate to reduce the heart'oxygen requirements while providing pacing therapies to maintain the patient's heart rate within acceptable limits, i.e. to overcome bradyarrhythmias and/or unphysiological AC-delays induced by the nerve stimulation.